When cells are stimulated by multiple factors (such as bacterial infection, oxidative stress, and antigenic immunity), IκBα is phosphorylated and rapidly degraded, and then NF-κB translocates to the nucleus to start transcriptional regulation, promoting the expression of key downstream inflammatory factors, such as TNF-α, IL-1β and IL-6; in turn, it initiates an inflammatory response [43]. This evidence concerns the gene NFKB1 and bacterial infectious disease.